drugs and addiction lect 2

Question 1

what is the biological basis of drugs

Answer 1

-introducing drug to the brain upsets the natural balance the brain is striving for
-brain seeks to minimise the effect of drug and restore homeostasis

Question 2

what is homeostasis in the brain called

Answer 2

neuroadaptation

Question 3

what are the 2 types of neurotransmission

Answer 3

agonists and antagonists

Question 4

what are agonists

Answer 4

-increase neural activity
-activate receptors either by mimicking the neurotransmitter or by increasing the existing neurotransmitter
-can also block reuptake

Question 5

what are antagonists

Answer 5

-decrease neural activity by blocking the activation of receptors

Question 6

what is tolerance

Answer 6

-when we use a drug repeatedly the effects diminish
-we need more and more to get the effects we had when we first used it
-applies to all drugs of abuse
-happens at diff rates and to varying extents for diff drugs
-neg effects like nausea of often have fastest tolerance

Question 7

what is the biology behind tolerance

Answer 7

-metabolic tolerance: the body becomes more efficient at breaking the drug down (pharmacokinetic tolerance) (small effect)

-cellular tolerance: (pharmacodynamic tolerance), change in no of receptors e.g downregulation in receptor function/ or post synaptic function (large effect)

Question 8

what are the primary effects of drugs

Answer 8

1.more alert and improve conc (caffeine)
2.decrease social inhibitions, relaxation and hedonism/pleasure (alcohol)
3.euphoria, confidence, increased energy, alertness (cocaine)
4.hallucinations, altered sensory perception, laughing (psychodelics)
5.altered sensory perception, energy, connection with others (MDMA, ecstasy)

Question 9

caffeine

Answer 9

-works on adenosine as antagonist
-block adenosine receptors
-adenosine = tiredness so high at night
-blocks GABA receptors but only in v high doses
-psychoactive substance
-mostly in tea and coffee but added into many soft drinks particularly in USA

Question 10

what are the pos effects of caffeine

Answer 10

+increases alertness when needed (smith et al)
+consumption of caffeine in simulated driving break reduced driver impairments and sleepiness when driving

Question 11

tolerance for caffeine

Answer 11

Evans and Griffiths
-daily caffeine or placebo
-caffeine cond = less sig subjective effects of caffeine than placebo cond

Shi et al
-chronic administration of caffeine in mice
-found upregulation of A adenosine receptors, serotonin receptors, GABA receptors and others
-down regulation of other receptors

Question 12

nicotine

Answer 12

-agonist effect on acetylcholine transmitters
-stimulates nicotine receptors of acetylcholine neurons
-most neg effects of smoking come from inhalation of tobacco rather than the nicotine

Question 13

nicotine pos effects

Answer 13

-performance enhancement e.g attention, protective attributes against health e.g ADHD, parkinsons etc
-BUT regular smoking is neg reinforced and governed by withdrawal

Question 14

alcohol

Answer 14

-acts on multiple neurotransmitters
-crosses BBB very quickly, detected in brain in minutes
-specific and non specific actions on brain

Question 15

non specific actions of alcohol on brain

Answer 15

acts as a depressant on all brain neurons and disturbs neuronal membrane lipids (membrane fluidisation)

Question 16

primary specific mechanisms of action of alcohol

Answer 16

-inhibits glutamate by reducing effectiveness at NMDA glutamate receptor
-stimulates GABA release
-increases GABA receptor sensitivity, depressing neural system (leads to sedation)
-enhances endorphin activity in dopaminergic reward pathways leading to disinhibition of dopamine release in nucleus accumbens
-effects serotenergic neurotransmitters impacting general state of wellbeing

Question 17

alcohol and sugar

Answer 17

-sugar dependent rats increased intake of alcohol when deprived of access to sugar (Avena 2004)
-access to alcohol increased sugar intake in rats
-bingeing on either sugar or alcohol fostered the intake of the other (implications for human diet and alcohol intake)

Question 18

cannabis

Answer 18

-active ingredient is delta 9-THC and CBD
-only THC is psychoactive
- cannabinoid receptors identified in brain only responsive to cannabis, specifically the THC
-found anandamide which is an endogenous cannabinoid (decreases GABA and increases synaptic dopamine levels)

Question 19

what does repeated use of cannabis cause

Answer 19

-linked with interaction between THC and presynaptic CB1 receptors on inhibitory GABAergic interneurons in reward pathway
(reduction in release of GABA: disinhibition of dopaminergic neurons and elevation in synaptic dopamine levels

Question 20

changing the landscape of cannabis use

Answer 20

-legal for recreational use in many places e.g canada, africa, thailand etc
-decriminalised in netherlands and portugal
-legal for medical use in 49 countries including UK
-hardly prescribed at all in uK

Question 21

reasons for legalisation of cannabis

Answer 21

1.adverse health effects from cannabis are quite modest in relation to other drugs
2.criminal penalties for cannabis are harmful to users and the community and outweigh the neg consequences of using the drug (what is the benefit of criminalising people who use cannabis for personal use? waste of money and resources?)
3.if legal, cannabis can be better monitored and taxed

Question 22

Chiu et al research

Answer 22

-systematic review of trends in US attitudes towards cannabis legalisation
-attitudes were liberal across most demographic groups
-key findings contributing to more liberal views in general public:
–increase in no of people who use cannabis
–decrease in religious views
–increase in political liberalism
–decrease in perceived harmfulness of cannabis

Question 23

strength of cannabis for medical use

Answer 23

+good evidence for cannabis for medical uses, relief of chronic pain, neuropathic pain, spasticity can be eased (hill 2015)

Question 24

risks of cannabis for medical use

Answer 24

-clear but small risk for psychosis (Murray), worse for synthetic cannabinoids e.g spice
-mixed evidence about whether cannabis is carcinogenic (cancer causing)
-addiction and gateway risk (Volkow 2014), once you use one drug you are likely to try another, and you know people who may encourage use of other drugs

Question 25

synthetic cannabinoids (spice)

Answer 25

-acts similarly to cannabis
- doesnt have CBD but has THC
-lack of CBD = prevents mediating or relaxing effects in comparison to natural cannabis, more neg effects and less pos effects
-cause agitation, irritability, confusion, hallucinations and psychosis

Question 26

heroin and opioids

Answer 26

-heroin is a types of opioid
-pert and snyder found specific opioid receptors (there is a substance in brain that acts like opioids)
-opiates like heroin and morphine mimic endorphins (sit in receptor sites of endogenous opioids such as endorphins)
-synaptic dopamine levels (due to disinhibition of dopaminergic neurons) involved in reward mechanism of the drug
-very addictive in physical and psychological sense

Question 27

heroin and tolerance

Answer 27

-quick tolerance to nausea often experienced with opioids
-no tolerance ever to constipation or pin point pupils

Question 28

tolerance and overdose

Answer 28

-overdose happens when people on road to recovery
-tolerance has gone down but indiv use a habitual amount which is too much following abstinence or reduction (White and Irvine 1999)

Question 29

cocaine

Answer 29

-blocks reuptake of dopamine, noradrenaline and serotonin
-acts as agonist to neurotransmitters by blocking reuptake so increases neurotransmitters
-addictive potential correlated with increased dopaminergic activity in mesocorticolimbic pathways

Question 30

amphetamines

Answer 30

-stimulate release of DA so are DA agonists
-stimulates release of noradrenaline
-methamphetamine increases synaptic levels of monoamines (noradrenaline, serotonin and dopamine)
-impairs active transport of monoamines into synaptic vesicles
-slows catecholamine metabolism and inhibits dopamine synthesis
-increases level of dopamine and noradrenaline but has hallucinogenic effect

Question 31

ecstasy and MDMA

Answer 31

-hallucinogen due to effect on perception of reality
-stimulates release of noradrenaline and serotonin and dopamine

Question 32

other hallucinogens and what are they

Answer 32

-LSD, magic mushrooms and psychodelic drugs
-powerfully alter cog, mood, perception
-not addictive
-serotonin agonists as main action

Question 33

MDMA research on therapeutic benefits

Answer 33

-alcohol dependence, PTSD, social anxiety

Question 34

psychedelic research on therapeutic benefits

Answer 34

anxiety, depression, substance misuse

Question 35

therapeutic uses of MDMA and psilocybin

Answer 35

-licensed in 2023 in australia for prescription in psychiatric cases (MDMA for PTSD, psilocybin for treatment of resistant depression)
-psilocybin = good efficacy for use with controlled therapy on depression and PTSD
-action through agonism of certain receptors increasing connections in serotonin pathways e.g feeling connected, safety and positivity

Question 36

ketamine

Answer 36

-acts on CNS
-local anaesthetic properties
-antagonist of NDMA (primary mechanism of anaesthetic and analgesic action of ketamine)
-reduced presynaptic release of glutamate
-evidence for ketamine as antidepressant
-can improve mood and reduce suicidality
(licensed for treatment of depression in USA)

Question 37

benzodiazepines

Answer 37

-prescription medication that is abused
-agonist for GABA leading to muscle relaxation
-can block adenosine reuptake decreasing arousal and increasing sleepiness